Researchers find potential path to repair MS-damaged nerves

January 11, 2018

Gene expression in specific cells and in specific regions can provide a more precise neuroprotective approach than traditional treatments for multiple sclerosis. Increasing cholesterol synthesis gene expression in astrocytes of the spinal cord can be a pathway to repair nerves that affect walking.

Working with a mouse model of MS, UCLA researchers assessed astrocytes in various regions of the brain and spinal cord known to be involved in walking, vision, or cognition. Astrocytes are star-shaped cells in the brain and spinal cord that perform many functions including biochemical support of endothelial cells that form the blood-brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance. Atrocytes also have a role in the repair and scarring process of the brain and spinal cord following traumatic injuries.

The researchers compared gene expression changes between regions linked to different disabilities. In the spinal cord, they found a decrease in the expression of cholesterol synthesis genes. Cholesterol does not leave the blood and enter the brain, instead it is made in astrocytes and plays a role in making myelin and synapses. They hypothesized that while inflammation causes loss of myelin and synapses, it is the decrease in cholesterol synthesis gene expression in astrocytes that explains why lesions do not repair in MS. They treated MS mice with a drug that increased expression in cholesterol synthesis genes – and this resulted in improved walking ability.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the researchers said this disability-specific discovery approach represents a strategy for finding neuroprotective treatments for neurodegenerative diseases that are tailored to repair damage for each disability, one at a time, in contrast to a "one size fits all" treatment approach.

The study was published in the Proceedings of the National Academy of Sciences.